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Cancers
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The Role of Mitochondrial Ion Channels and Transporters in Cancer...
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The Role of Mitochondrial Ion Channels and Transporters in Cancer Development and Progression

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 9477

Special Issue Editors

Prof. Dr. Luigi Leanza

E-Mail Website
Guest Editor
Intracellular Ion Channel Group, Department of Biology, Università degli Studi di Padova, Padova, Italy
Interests: mitochondria; Wnt signaling; ER-mitochondria contact sites; cancer
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Ildiko Szabo

E-Mail Website
Guest Editor
Intracellular Ion Channel Group, Department of Biology, Università degli Studi di Padova, Padova, Italy
Interests: ion channels; mitochondria; cancer; pharmacological targeting
Dr. Vanessa Checchetto

E-Mail Website
Guest Editor
Intracellular Ion Channel Group, Department of Biology, Università degli Studi di Padova, Padova, Italy
Interests: ion channels; mitochondria; electrophysiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ion channels and transporters play an important role in modulating cellular functions and in determining cell fate. Recent evidence has demonstrated that plasma membrane as well as intracellular ion transporting proteins are involved in cancer progression and in the acquisition of the main malignant features by cancer cells, such as metabolic reprogramming, absence of proliferative control, resistance to cell death induction, stimulation of angiogenesis, migration and invasion abilities. In this scenario, an important role is mediated by mitochondrial ion channels and transporters.

These channels are involved in fine-tuning the mitochondrial membrane potential and reactive oxygen species (ROS) production and thus regulate mitochondrial physiology, which in turn impacts several hallmarks of cancer. Significantly, ion transport can be modulated by several synthetic compounds or natural products, which allows a great variety of pharmacological options to regulate the function of proteins mediating ion transport and reduce tumor progression, as illustrated in preclinical mouse tumor models.

In this Special Issue, we welcome reviews, descriptions of new analytical methods, and original articles covering various aspects of the pathophysiology and pharmacological targeting of mitochondrial ion channels in cancer. We hope that this Special Issue will delineate future perspectives in the field and prompt further investigation.

We look forward to your contributions.

Prof. Dr. Luigi Leanza
Prof. Dr. Ildikò Szabò
Dr. Vanessa Checchetto
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondria
  • ion channels
  • ion transporters
  • cancer
  • signaling
  • cell death
  • pharmacology

Published Papers (3 papers)

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Research

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16 pages, 1840 KiB  
Article
Mitochondrial Kv1.3 Channels as Target for Treatment of Multiple Myeloma
by Stephanie Kadow, Fabian Schumacher, Melanie Kramer, Gabriele Hessler, René Scholtysik, Sara Oubari, Patricia Johansson, Andreas Hüttmann, Hans Christian Reinhardt, Burkhard Kleuser, Mario Zoratti, Andrea Mattarei, Ildiko Szabò, Erich Gulbins and Alexander Carpinteiro
Cancers 2022, 14(8), 1955; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14081955 - 13 Apr 2022
Cited by 7 | Viewed by 1878
Abstract
Despite several new developments in the treatment of multiple myeloma, all available therapies are only palliative without curative potential and all patients ultimately relapse. Thus, novel therapeutic options are urgently required to prolong survival of or to even cure myeloma. Here, we show [...] Read more.
Despite several new developments in the treatment of multiple myeloma, all available therapies are only palliative without curative potential and all patients ultimately relapse. Thus, novel therapeutic options are urgently required to prolong survival of or to even cure myeloma. Here, we show that multiple myeloma cells express the potassium channel Kv1.3 in their mitochondria. The mitochondrial Kv1.3 inhibitors PAPTP and PCARBTP are efficient against two tested human multiple myeloma cell lines (L-363 and RPMI-8226) and against ex vivo cultured, patient-derived myeloma cells, while healthy bone marrow cells are spared from toxicity. Cell death after treatment with PAPTP and PCARBTP occurs via the mitochondrial apoptotic pathway. In addition, we identify up-regulation of the multidrug resistance pump MDR-1 as the main potential resistance mechanism. Combination with ABT-199 (venetoclax), an inhibitor of Bcl2, has a synergistic effect, suggesting that mitochondrial Kv1.3 inhibitors could potentially be used as combination partner to venetoclax, even in the treatment of t(11;14) negative multiple myeloma, which represent the major part of cases and are rather resistant to venetoclax alone. We thus identify mitochondrial Kv1.3 channels as druggable targets against multiple myeloma. Full article
(This article belongs to the Special Issue The Role of Mitochondrial Ion Channels and Transporters in Cancer Development and Progression)
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16 pages, 3518 KiB  
Article
Kv1.3 Controls Mitochondrial Dynamics during Cell Cycle Progression
by Jesusa Capera, Mireia Pérez-Verdaguer, María Navarro-Pérez and Antonio Felipe
Cancers 2021, 13(17), 4457; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13174457 - 04 Sep 2021
Cited by 4 | Viewed by 2259
Abstract
The voltage-gated potassium channel Kv1.3 is a potential therapeutic target for obesity and diabetes. The genetic ablation and pharmacological inhibition of Kv1.3 lead to a lean phenotype in rodents. The mechanism of regulation of body weight and energy homeostasis involves Kv1.3 expression in [...] Read more.
The voltage-gated potassium channel Kv1.3 is a potential therapeutic target for obesity and diabetes. The genetic ablation and pharmacological inhibition of Kv1.3 lead to a lean phenotype in rodents. The mechanism of regulation of body weight and energy homeostasis involves Kv1.3 expression in different organs, including white and brown adipose tissues. Here, we show that Kv1.3 promotes the proliferation of preadipocytes through the control of mitochondrial dynamics. Kv1.3 is expressed in mitochondria exhibiting high affinity for the perinuclear population. The mitochondrial network is highly dynamic during the cell cycle, showing continuous fusion-fission events. The formation of a hyperfused mitochondrial network at the G1/S phase of the cell cycle is dependent on Kv1.3 expression. Our results demonstrate that Kv1.3 promotes preadipocyte proliferation and differentiation by controlling mitochondrial membrane potential and mitochondrial dynamics at the G1 phase of the cell cycle. Full article
(This article belongs to the Special Issue The Role of Mitochondrial Ion Channels and Transporters in Cancer Development and Progression)
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Review

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16 pages, 1807 KiB  
Review
Glutamine-Derived Aspartate Biosynthesis in Cancer Cells: Role of Mitochondrial Transporters and New Therapeutic Perspectives
by Ruggiero Gorgoglione, Valeria Impedovo, Christopher L. Riley, Deborah Fratantonio, Stefano Tiziani, Luigi Palmieri, Vincenza Dolce and Giuseppe Fiermonte
Cancers 2022, 14(1), 245; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14010245 - 04 Jan 2022
Cited by 14 | Viewed by 4433
Abstract
Aspartate has a central role in cancer cell metabolism. Aspartate cytosolic availability is crucial for protein and nucleotide biosynthesis as well as for redox homeostasis. Since tumor cells display poor aspartate uptake from the external environment, most of the cellular pool of aspartate [...] Read more.
Aspartate has a central role in cancer cell metabolism. Aspartate cytosolic availability is crucial for protein and nucleotide biosynthesis as well as for redox homeostasis. Since tumor cells display poor aspartate uptake from the external environment, most of the cellular pool of aspartate derives from mitochondrial catabolism of glutamine. At least four transporters are involved in this metabolic pathway: the glutamine (SLC1A5_var), the aspartate/glutamate (AGC), the aspartate/phosphate (uncoupling protein 2, UCP2), and the glutamate (GC) carriers, the last three belonging to the mitochondrial carrier family (MCF). The loss of one of these transporters causes a paucity of cytosolic aspartate and an arrest of cell proliferation in many different cancer types. The aim of this review is to clarify why different cancers have varying dependencies on metabolite transporters to support cytosolic glutamine-derived aspartate availability. Dissecting the precise metabolic routes that glutamine undergoes in specific tumor types is of upmost importance as it promises to unveil the best metabolic target for therapeutic intervention. Full article
(This article belongs to the Special Issue The Role of Mitochondrial Ion Channels and Transporters in Cancer Development and Progression)
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